Homo sapiens
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PROVIDER: PRJNA103911 | ENA |
REPOSITORIES: ENA
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Project description:Direct comparison of the genome-level expression patterns of THP-1 cells exposed to either LPS or heat shock; Peripheral blood mononuclear cells (PBMC) serve a sentinel role allowing the host to efficiently sense and adapt to the presence of danger signals. Herein we have directly compared the genome-level expression patterns (microarray) of human PBMC (THP-1 cells) subjected to one of two canonical danger signals, heat shock and lipopolysaccharide (LPS). Based on sequential expression and statistical filters, and in comparison to control cells, we found that 3,988 genes were differentially regulated in THP-1 cells subjected to LPS stress, and 2,921 genes were differentially regulated in THP-1 cells subjected to heat shock stress. Venn analyses demonstrated that the majority of differentially regulated genes (greather than or equal to 70%) were uniquely expressed in response to one of the two danger signals. Functional analyses demonstrated that the two danger signals induced expression or repression of genes corresponding to unique pathways, molecular functions, biological processes, and gene networks. In contrast, there were 184 genes that were commonly upregulated by both stress signals, and 430 genes that were commonly downregulated by both stress signals. Interestingly, the 184 commonly upregulated genes corresponded to a gene network broadly related to inflammation, and more specifically to chemokine signaling. These data demonstrate that the mononuclear cell responses to the canonical stress signals, heat shock and LPS, are highly divergent. However, there is a heretofore unrecognized common pattern of gene network expression corresponding to chemokine-related biology. The data also serve as a reference database for investigators in the field of stress signaling. Experiment Overall Design: In vitro exposure of THP-1 cells to control conditions, LPS (1 micogram/ml for 4 hrs), or heat shock (43 deg C for 1 hour, followed by a 4 hour recovery at 37 deg C)
2008-06-20 | E-GEOD-9916 | biostudies-arrayexpress
Project description:Direct comparison of the genome-level expression patterns of THP-1 cells exposed to either LPS or heat shock Peripheral blood mononuclear cells (PBMC) serve a sentinel role allowing the host to efficiently sense and adapt to the presence of danger signals. Herein we have directly compared the genome-level expression patterns (microarray) of human PBMC (THP-1 cells) subjected to one of two canonical danger signals, heat shock and lipopolysaccharide (LPS). Based on sequential expression and statistical filters, and in comparison to control cells, we found that 3,988 genes were differentially regulated in THP-1 cells subjected to LPS stress, and 2,921 genes were differentially regulated in THP-1 cells subjected to heat shock stress. Venn analyses demonstrated that the majority of differentially regulated genes (greather than or equal to 70%) were uniquely expressed in response to one of the two danger signals. Functional analyses demonstrated that the two danger signals induced expression or repression of genes corresponding to unique pathways, molecular functions, biological processes, and gene networks. In contrast, there were 184 genes that were commonly upregulated by both stress signals, and 430 genes that were commonly downregulated by both stress signals. Interestingly, the 184 commonly upregulated genes corresponded to a gene network broadly related to inflammation, and more specifically to chemokine signaling. These data demonstrate that the mononuclear cell responses to the canonical stress signals, heat shock and LPS, are highly divergent. However, there is a heretofore unrecognized common pattern of gene network expression corresponding to chemokine-related biology. The data also serve as a reference database for investigators in the field of stress signaling. Keywords: treated vs non treated
2007-12-18 | GSE9916 | GEO
Project description:The molecular mechanisms by which individuals subjected to environmental heat stress either adapt or develop heat-related complications are not well understood. We analysed the changes in blood mononuclear gene expression patterns in human volunteers exposed to an extreme heat in a sauna (temperature of 78 ± 6 °C).
2017-09-14 | GSE90763 | GEO
Project description:The molecular mechanisms by which individuals subjected to environmental heat stress either adapt or develop heat-related complications are not well understood. We analysed the changes in blood mononuclear gene expression patterns in human volunteers exposed to an extreme heat in a sauna (temperature of 78 ± 6 °C).
2017-11-01 | E-MTAB-6212 | biostudies-arrayexpress
Project description:Yeast Saccharomyces cerevisiae has been widely used as a model system for studying genomic instability. In this study, heat-shock-induced genomic alterations were explored in the heterozygous diploid yeast strain JSC25-1. In combination of the whole-genome microarray, the patterns of chromosomal instability induced by heat shock could also be explored at a whole genome level. Using this system, we found heat-shock treatment resulted in hundreds-fold higher rate of genomic alterations, including aneuploidy and loss of heterozygosity (LOH).
2020-05-18 | GSE150711 | GEO
Project description:Environmental stress, such as oxidative or heat stress, induces the activation of the heat shock response
(HSR) and leads to an increase in the heat shock proteins (HSPs) level. These HSPs act as molecular
chaperones to maintain cellular proteostasis. Controlled by highly intricate regulatory mechanisms,
having stress-induced activation and feedback regulations with multiple partners, the HSR is still
incompletely understood. In this context, we propose a minimal molecular model for the gene
regulatory network of the HSR that reproduces quantitatively different heat shock experiments both
on heat shock factor 1 (HSF1) and HSPs activities. This model, which is based on chemical kinetics
laws, is kept with a low dimensionality without altering the biological interpretation of the model
dynamics. This simplistic model highlights the titration of HSF1 by chaperones as the guiding line of
the network. Moreover, by a steady states analysis of the network, three different temperature stress
regimes appear: normal, acute, and chronic, where normal stress corresponds to pseudo thermal
adaption. The protein triage that governs the fate of damaged proteins or the different stress regimes
are consequences of the titration mechanism. The simplicity of the present model is of interest in
order to study detailed modelling of cross regulation between the HSR and other major genetic
networks like the cell cycle or the circadian clock.
Sivéry, A., Courtade, E., Thommen, Q. (2016). A minimal titration model of the mammalian dynamical heat shock response. Physical biology, 13(6), 066008.
2022-01-25 | MODEL2201210001 | BioModels
Project description:Proteotoxic stress such as heat shock causes heat-shock factor (HSF)-dependent transcriptional upregulation of chaperones. Heat shock also leads to a rapid and reversible downregulation of many genes, a process we term stress-induced transcriptional attenuation (SITA). The mechanism underlying this conserved phenomenon is unknown. Here we report that enhanced recruitment of negative transcription elongation factors to gene promoters in human cell lines induces SITA. A chemical inhibitor screen showed that active translation and protein ubiquitination are required for the response. We further find that proteins translated during heat shock are subjected to ubiquitination and that p38 kinase signaling connects cytosolic translation with gene downregulation. Notably, brain samples of subjects with Huntington's disease also show transcriptional attenuation, which is recapitulated in cellular models of protein aggregation similar to heat shock. Thus our work identifies an HSF-independent mechanism that links nascent-protein ubiquitination to transcriptional downregulation during heat shock, with potential ramifications in neurodegenerative diseases.
2019-02-07 | GSE112379 | GEO
Project description:We examined the stress response in Entamoeba histolytica trophozoites by comparing untreated log-phase HM-1:IMSS trophozoites to those subjected to heat shock at 42C for 1 hour. Keywords: stress reponse We compared two arrays from normal trophozoites to two arrays from trophozoites subjected to heat shock.
2007-03-01 | E-GEOD-6650 | biostudies-arrayexpress
Project description:We examined the stress response in Entamoeba histolytica trophozoites by comparing untreated log-phase HM-1:IMSS trophozoites to those subjected to heat shock at 42C for 1 hour. Keywords: stress reponse
2007-03-01 | GSE6650 | GEO
Project description:Cells respond to many different types of stresses by overhauling gene expression patterns, both at the transcriptional and translational level. Under heat stress, global transcription and translation are inhibited, while the expression of chaperone proteins are preferentially favored. As the direct link between mRNA transcription and protein translation, tRNA expression is intricately regulated during the stress response. Despite extensive research into the heat shock response (HSR), the regulation of tRNA expression by RNA Polymerase III (Pol III) transcription has yet to be fully elucidated in mammalian cells. Here, we examine the regulation of Pol III transcription during different stages of heat shock stress in mouse embryonic stem cells (mESCs). We observe that global transcription of tRNAs is downregulated after 30 minutes of heat shock, followed by an overall increase in tRNA transcription after 60 minutes of heat shock. This effect is more evident in tRNAs, though other RNA Pol III gene targets are also similarly affected. Notably, we show that the down-regulation at 30 minutes of heat shock is independent of HSF1, the master transcription factor of the HSR, but that the subsequent increase in expression at 60 minutes requires HSF1. Taken together, these results demonstrate an adaptive RNA Pol III response to heat stress, and an intricate relationship between the canonical HSR and tRNA expression.
2025-03-04 | GSE282678 | GEO